Jose G. Merino, MD, MPhil

Disclosures

May 20, 2016

Brain-Machine Interface Technology

Brain-machine interface (BMI) technology is rapidly evolving and may one day offer hope to patients with the most disabling neurologic conditions. Invasive BMI technology detects neural activity using multielectrode arrays (MEAs) inserted directly onto cortical tissue or electrocorticography (ECoG) electrodes placed on the cortical surface. A signal processor decodes these neural signals and uses the information to move a robotic limb or a communication device (a screen cursor, a keyboard, or a speech synthesizer).

Recent clinical research experience suggests that these devices improve the quality of life of patients with serious neurologic conditions. Since the turn of the century, experiments in patients who were locked-in because of ALS or a brainstem stroke showed that MEAs allow volitional control of a cursor. Since then, further refinements in BMI technology, including work done by Karunesh Ganguly, MD, PhD,[1] assistant professor of neurology at the University of California, San Francisco, allow patients with tetraparesis to control the x and y positions of a cursor on the screen and reach, grasp, and move objects using a robotic arm. BMI technology has also allowed locked-in patients with ALS to control spelling devices and use a keyboard and a speech synthesizer. There are also intriguing animal data[4] that suggest that learning to use these devices may promote cortical network changes and neuroplasticity, but the clinical implications for patients are still unknown.

Deep Brain Stimulation for Alzheimer Disease

Because it modulates the activity of widespread cortical-subcortical circuits important for motor control, deep brain stimulation (DBS) has been used to treat patients with movement disorders for decades. With greater understanding of how these circuits modulate brain activity, the indications for DBS (clinically and for research purposes) are expanding and now include epilepsy, headache, depression, obsessive-compulsive disorder, and other neuropsychiatric conditions, including Alzheimer disease (AD).

One approach to DBS in AD relies on stimulation of the nucleus basalis of Meynert to modulate cholinergic function. Another approach is stimulation of the fornix to modulate the activity of the circuit of Papez. This second approach was evaluated by Andres Lozano, MD, PhD, FRCSC, BMedSci, senior scientist at the Krembil Research Institute and a neurosurgeon at Toronto Western Hospital and his team in a phase 1 trial[5] of six patients with mild AD who underwent continuous stimulation for a year. Using low-resolution electromagnetic tomography, Lozano and his team found that DBS drove neural activity in the memory circuit. PET scans showed an early and striking reversal of the impaired glucose utilization in the temporal and parietal lobes. And some patients had mild improvement in standardized cognition tests. Based on these results, they started a phase 2 trial that enrolled 42 patients to evaluate the safety of DBS in patients with mild Alzheimer disease; the study is ongoing but not recruiting patients. In a different study,[6] these investigators found that after 1 year of DBS, the hippocampus volume increased in some patients, replicating findings from animal studies[7] that, in addition, found that stimulation of the fornix led to an increase in neurotrophic factors, neurogenesis, and increased dendritic arborization. These findings raise very exciting hypotheses regarding neuroplasticity even in patients with neurodegenerative conditions and the long-term effects of DBS.

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